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  • 1
    Electronic Resource
    Electronic Resource
    Beneficial Effects of Captopril and Metoprolol Treatment in Idiopathic Dilated Cardiomyopathy (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of noninvasive electrocardiology 1 (1996), S. 0 
    Details
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Abnormal autonomic nervous function (ANF), such as an enhanced sympathetic tone and an attenuated parasympathetic tone, have been shown in patients with congestive heart failure (CHF).Methods: We examined the effects of captopril and metoprolol on autonomic nervous function and ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy (DCM), using 24-hour ambulatory electrocardiographic monitoring and power spectral analysis of heart rate variability. Twenty-one patients (pts) with idiopathic DCM (54 ± 15 years [mean ± SDI) were allocated to three groups: a captopril group (8 pts); a metoprolol group (7 pts); and a control group (6 pts). Power spectra were quantified in high (HF) and low frequency power (LF), and natural logarithmic values of HF (In(HF) and LF/HF (In (LF(HF]) were used as indices of parasympathetic and sympathetic nervous activities, respectively.Results: In the captopril and the metoprolol groups, there was a significant increase in In(HF) (P 〈 0.05), a trend of decrease in ln(LF/HF), and an improvement of ventricular arrhythmia (VA). In contrast, no significant change was found in any of In(HF), In (LF/HF), and VA in the control group.Conclusion: We conclude that both captopril and metoprolol have beneficial effects on ANF and VA, and the restored autonomic balance and the improvement of VA correlate to each other.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1542-474X.1996.tb00295.x
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  • 2
    Electronic Resource
    Electronic Resource
    Positional Ventricular Tachycardia (2004)
    350 Main Street , Malden , MA 02148-5018 , USA and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Pacing and clinical electrophysiology 27 (2004), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A 60-year-old man showed nonsustained repetitive monomorphic VT in the left lateral position, but this was terminated by deep inspiration. Echocardiography and MRI demonstrated a false tendon extending from the apex to the basal septum where the VT could have originated. Spontaneous remission occurred during the16-year follow-up.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.2004.00650.x
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  • 3
    Electronic Resource
    Electronic Resource
    Activation of the ERK/MAPK pathway by an isoform of rap1GAP associated with Gα i (1999)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 400 (1999), S. 891-894 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Many receptors for neuropeptides and hormones are coupled with the heterotrimeric Gi protein, which activates the p42/44 mitogen-activated protein kinase (ERK/MAPK) cascade through both the α- and βγ-subunits of Gi (refs 1–3). The ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/23738
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  • 4
    Electronic Resource
    Electronic Resource
    The MHC class I-like Zn-α2-glycoprotein gene maps to mouse chromosome 5 (1995)
    Springer
    Immunogenetics 42 (1995), S. 72-74 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00164991
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  • 5
    Electronic Resource
    Electronic Resource
    Increased calcium release from sarcoplasmic reticulum stimulated by inositol trisphosphate in spontaneously hypertensive rat heart cells (1993)
    Springer
    Molecular and cellular biochemistry 119 (1993), S. 51-57 
    Details
    ISSN: 1573-4919
    Keywords: Inositol-1, 4, 5-trisphosphate ; sarcoplasmic reticulum ; calcium release ; cardiac hypertrophy ; PI-response ; cardiac myocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract It is known that inositol (1, 4, 5)-trisphosphate (IP3) stimulates Ca2+ release from sarcoplasmic reticulum (SR) in several tissues, but in cardiac myocytes this phenomenon has not been confirmed. The purpose of the present study was to confirm the effect of (1, 4, 5)-IP3 on Ca2+ release from SR in cardiac myocytes. The effect of IP3 on Ca2+ release from SR in hypertrophic cardiac cells was also determined. We examined the effects of IP3 on Ca2+ release from cardiac myocyte SR by the bigital-image method in a single cell. We also determined the effect of IP3 on calcium release from isolated SR. SR was prepared from spontaneous hypertensive rat hearts and Wistar kyoto rat hearts. The SR was prelabeled with45Ca2+, and then incubated with the indicated concentrations of IP3 for 1 min at 37°C. In cardiac myocytes treated with saponin, Ca2+ release stimulated by 10 μM (1, 4, 5)-IP3 was detected by fura-2. In45Ca2+ prelabeled SR, the maximal Ca2+ release was achieved at 10 μM IP3 incubated for 1 min. The release of Ca2+ was higher in Sr of SHR than in the SR of WKY. IP3 stimulates Ca2+ release from cardiac SR, and this release is greater in SHR than in WKY. However, it is uncertain whether this phenomenon plays a role in cardiac hypertrophy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926853
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  • 6
    Electronic Resource
    Electronic Resource
    Distribution of angiotensinogen in diseased human hearts (1994)
    Springer
    Molecular and cellular biochemistry 132 (1994), S. 15-23 
    Details
    ISSN: 1573-4919
    Keywords: angiotensinogen ; atrial natriuretic peptide ; immunohistochemistry ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Extrahepatic synthesis and localization of angiotensinogen (ATN) have been described in animals, thus establishing the tissue renin-angiotensin (RA) system. However, there had been no reports of tissue RA systems in human organs, including the heart. In earlier, we have reported the possibility of ATN synthesis in the human heart using ribonuclease protection assay system. ATN mRNA was detected not only in the liver, but also in both the atrial and ventricular heart tissues, suggesting that ATN is synthesized in the human heart. In this report, we looked for the distribution of ATN in diseased human heart. Northern blot hybridization of cDNA with total RNA extracted from human liver, brain, kidney, atrial and ventricular tissues revealed that ATN mRNA exists in cardiac ventricule. Immunohistochemical studies using a specific antibody to ATN revealed a stronger reaction in the endocardial layer of the human left ventricle, than in the epicardial layer, and intense immunoreactivity in the conduction system and right atrium. This distribution pattern was similar to that of human atrial natriuretic peptide (hANP), which functions a smooth muscle relaxant. Double immunostaining of ATN and hANP demonstrated that all myocytes in the right atrium had immunopositive reactions to ATN, hANP or both of ATN and hANP. Double immunoelectron staining enabled us to show more detailed localization of ATN and hANP; hANP only existed in the specific granules and ATN existed in the myofibril, but not in the granule. Furthermore, our experiments provide evidence of ATN in healthy human hearts and also reveal a widespread immunopositive reaction for ATN in the left ventricle of diseased hearts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00925670
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  • 7
    Electronic Resource
    Electronic Resource
    Increased mRNA expression of cardiac renin-angiotensin system and collagen synthesis in spontaneously hypertensive rats (1998)
    Springer
    Molecular and cellular biochemistry 178 (1998), S. 51-58 
    Details
    ISSN: 1573-4919
    Keywords: cardiac hypertrophy ; angiotensin II ; collagen ; renin-angiotensin system ; spontaneously hypertensive rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Hypertensive cardiac hypertrophy is associated with the accumulation of collagen in the myocardial interstitium. Previous studies have demonstrated that this myocardial fibrosis accounts for impaired myocardial stiffness and ventricular dysfunction. Although cardiac fibroblasts are responsible for the synthesis of fibrillar collagen, the factors that regulate collagen synthesis in cardiac fibroblasts are not fully understood. We investigated the effects of angiotensin II on cardiac collagen synthesis in cardiac fibroblasts. Cardiac fibroblasts of 10 week old spontaneously hypertensive rats and age-matched Wistar-Kyoto rats were prepared and maintained in culture medium supplemented with 10% fetal calf serum. The expression of mRNA of the renin-angiotensin system (renin, angiotensinogen, angiotensin converting enzyme) was determined by using a ribonuclease protection assay. Basal collagen synthesis in cardiac fibroblasts from spontaneously hypertensive rats was 1.6 fold greater than that in the cell of Wistar-Kyoto rats. Angiotensin II stimulated collagen synthesis in cardiac fibroblasts in a dose-dependent manner. The responsiveness of collagen production to angiotensin II was significantly enhanced in cardiac fibroblasts from spontaneously hypertensive rats (100 nM angiotensin II resulted in 185 ± 18% increase above basal levels, 185 ± 18 versus 128 ± 19% in Wistar-Kyoto rats p 〈 0.01). This effect was receptor-specific, because it was blocked by the competitive inhibitor saralasin and MK 954. These results indicate that collagen production was enhanced in cardiac fibroblasts from spontaneously hypertensive rats, that angiotensin II had a stimulatory effect on collagen synthesis in cardiac fibroblasts, and that cardiac fibroblasts from spontaneously hypertensive rats were hyper-responsive to stimulation by angiotensin II. Level of angiotensin and renin mRNA expressed in ventricles, and angiotensinogen mRNA expressed in fibroblasts from SHR were higher than those from WKY. These findings suggest that the cardiac renin-angiotensin system may play an important role in collagen accumulation in hypertensive cardiac hypertrophy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006830401072
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  • 8
    Electronic Resource
    Electronic Resource
    Alteration of extracellular matrix in dilated cardiomyopathic hamster heart (1996)
    Springer
    Molecular and cellular biochemistry 156 (1996), S. 9-15 
    Details
    ISSN: 1573-4919
    Keywords: collagen ; extracellular matrix ; reducible crosslink ; cardiomyopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The purpose of this study was to characterize the collagen in hereditary dilated cardiomyopathic hamster hearts, and to examine the participation of the collagen in the occurrence and progression of cardiomyopathy. BIO 53.58 hamsters (5, 10, 20 weeks old) were used as the model of dilated cardiomyopathy. Flb hamsters were used as controls. The collagen content was almost constant at any age in the Flb hamsters, but increased with age in BIO 53.58 hamsters. Type III collagen increased significantly in BIO 53.58 hamsters at 10 weeks. The acetic acid solubility of collagen decreased in BIO 53.58 hamsters as the fibrosis progressed, but was unchanged in controls. Reducible crosslinks showed a tendency to decrease progressively in BIO 53.58 hamsters. There were no differences between Flb and BIO 53.58 hamsters at 5 weeks, but its expression in BIO 53.58 hamsters at 10 and 20 weeks of age increased compared to Flb controls. These findings indicate that in the early phase of cardiomyopathy the extracellular matrix of the myocardium is rich in type III collagen. In the later phase, the matrix resembles that of hard tissues, whose collagen is mainly of type I collagen and is insoluble. These data suggest that the increased collagen synthesis may impair the cardiac function in the development of cardiomyopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00239313
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  • 9
    Electronic Resource
    Electronic Resource
    A possible model of the anginal syndrome with normal coronary arteriograms: Microembolization of canine coronary arteries (1987)
    Springer
    Heart and vessels 3 (1987), S. 7-13 
    Details
    ISSN: 1615-2573
    Keywords: Angina with normal coronary arteriogram ; Microsphere embolization ; Coronary micro-circulation ; Coronary flow reserve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate whether disseminative coronary embolization with microspheres brings about a pathophysiological mimicking of the syndrome of exertional angina with a normal coronary arteriogram, 25 dogs were studied immediately and 2 weeks after the coronary embolization with microspheres 15 µm [2.5×105 or 5.0×105/regional flow (ml/min)] and 25 µm [2.0×105/regional flow (ml/min)] in diameter. Two weeks after embolization with the 15-µm microspheres, the resting coronary blood flow recovered to the control (preembolization) level with the absence of myocardial necrosis, but the coronary flow reserve was significantly lower. In ten dogs receiving the larger dose embolization (5 × 105/regional flow (ml/min)), lactate production or a marked decrease in lactate extraction was observed during rapid atrial pacing. In five dogs subject to 25-µm microsphere embolization, however, disseminative patchy myocardial necrosis was observed and the coronary flow reserve remained normal. These results indicate that the chronic state after microembolization with a large dose of 15-µm microspheres mimics the syndrome of exertional angina with a normal coronary arteriogram, whereas 25-µm microsphere embolization does not. Thus, the condition of some patients with a normal coronary arteriogram but with reduced coronary flow reserve may be attributable to microcirculatory disturbances in the coronary arterioles or smaller vessels. Moreover, we observed that the coronary flow at the induction of myocardial ischemia by pacing was much less than the reactive hyperemic flow. This discrepancy may be a characteristic feature in this syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02073641
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  • 10
    Electronic Resource
    Electronic Resource
    Limited atrial compensation to reduced early diastolic filling in hypertensive patients with advanced left ventricular hypertrophy: A Doppler echocardiographic study (1989)
    Springer
    Heart and vessels 5 (1989), S. 33-40 
    Details
    ISSN: 1615-2573
    Keywords: Left ventricular filling ; Ventricular diastolic function ; Atrial function ; Left ventricular hypertrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess atrial contribution to left ventricular (LV) filling in hypertension, we studied, using pulsed Doppler echocardiography, 22 hypertensive patients without apparent LV hypertrophy (LVH), 12 hypertensive patients with LVH, and 24 age-matched normal subjects. From mitral flow velocity waveform, we determined peak velocity of early diastolic filling flow (peak E), peak velocity of late diastolic filling flow (peak A), and the peak A/peak E ratio (peak A/peak E). Peak E decreased in hypertensives without apparent LVH and showed a further decrease in hypertensives with LVH compared with normal subjects (57±8 [mean ± SD];P〈0.001, 46±7;P〈0.0001, vs 65±10 cm/s). On the other hand, peak A/peak E increased in hypertensives without apparent LVH, and greatly increased in hypertensives with LVH (1.06±0.14;P〈0.001, 1.40±0.29;P〈0.0001, vs 0.79±0.21). However, increased peak A was not significantly different between the hypertensive groups (60±8 vs 64±8; NS, both;P〈0.001 vs 50±10 cm/s for normal subjects). In hypertensives, we found no significant correlation between peak A and the wall thickness index (WTI, determined as mean LV wall thickness normalized by LV diastolic dimension), whereas peak E was significantly correlated with WTI (r=−0.65;P〈0.001). Our findings indicate that atrial contraction can not fully compensate the decrease in early diastolic filling caused by advanced LVH. We conclude that atrial compensation for reduced early diastolic filling is limited in hypertensive patients with advanced left ventricular hypertrophy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02058356
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